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Because depressive illness is recurrent, recurrence prevention should be a mainstay for reducing its burden on society. One way to reach this goal is to identify malleable risk factors. The ability to attenuate sadness/dysphoria (mood repair) and parasympathetic nervous system functioning, indexed as respiratory sinus arrhythmia (RSA), are impaired during depression and after it has remitted. The present study therefore tested the hypothesis that these two constructs also may mirror risk factors for a recurrent major depressive episode (MDE).
At time 1 (T1), 178 adolescents, whose last MDE had remitted, and their parents, reported on depression and mood repair; youths’ RSA at rest and in response to sad mood induction also were assessed. MDE recurrence was monitored until time 2 (T2) up to 2 years later. Mood repair at T1 (modeled as a latent construct), and resting RSA and RSA response to sadness induction (RSA profile), served to predict onset of first recurrent MDE by T2.
Consistent with expectations, maladaptive mood repair predicted recurrent MDE, above and beyond T1 depression symptoms. Further, atypical RSA profiles at T1 were associated with high levels of maladaptive mood repair, which, in turn, predicted increased risk of recurrent MDE. Thus, maladaptive mood repair mediated the effects of atypical RSA on risk of MDE recurrence.
This study documented that a combination of behavioral and physiological risk factors predicted MDE recurrence in a previously clinically referred sample of adolescents with depression histories. Because mood repair and RSA are malleable, both could be targeted for modification to reduce the risk of recurrent depression in youths.
While anxiety has been associated with exaggerated emotional reactivity, depression has been associated with blunted, or context insensitive, emotional responding. Although anxiety and depressive disorders are frequently co-morbid, surprisingly little is known about emotional reactivity when the two disorders co-occur.
We utilized the emotion-modulated startle (EMS) paradigm to examine the effects of a concurrent depressive episode on emotional reactivity in young adults with anxiety disorders. Using an archival dataset from a multi-disciplinary project on risk factors in childhood-onset depression, we examined eye-blink startle reactions to late-onset auditory startle probes while participants viewed pictures with affectively pleasant, unpleasant and neutral content. EMS response patterns were analyzed in 33 individuals with a current anxiety (but no depressive) disorder, 24 individuals with a current anxiety disorder and co-morbid depressive episode and 96 healthy controls.
Control participants and those with a current anxiety disorder (but no depression) displayed normative linearity in startle responses, including potentiation by unpleasant pictures. By contrast, individuals with concurrent anxiety and depression displayed blunted EMS.
An anxiety disorder concurrent with a depressive episode is associated with reactivity that more closely resembles the pattern of emotional responding that is typical of depression (i.e. context insensitive) rather than the pattern that is typical for anxiety (i.e. exaggerated).
Clinical depression involves persistent dysphoria, implicating impaired affect regulation or mood repair failure. However, there is comparatively little information about the mood repair repertoires of individuals with histories of clinical depression, how their repertories differ from that of never-depressed people, and whether particular types of mood repair responses differentially contribute to depression risk.
Adult probands who had childhood-onset depressive disorder (n=215) and controls with no history of major mental disorder (n=122) reported which specific (cognitive, behavioral, interpersonal and somatic-sensory) responses they typically deploy when experiencing sad affect, including responses known to appropriately attenuate dysphoria (‘adaptive’ responses) and those known to exacerbate dysphoria in the short or long run (‘maladaptive’ responses). Subjects were longitudinally followed and evaluated.
Remitted probands and probands in depressive episodes both reported a greater number of maladaptive responses and fewer adaptive responses to their own sadness than did controls, although probands did not have an absolute deficiency of adaptive responses. Maladaptive (but not adaptive) mood repair responses predicted future increases in depression symptoms and an increased probability of a recurrent depressive episode among probands (even after controlling for several clinical predictors of course). Post-hoc analyses revealed that maladaptive non-cognitive and maladaptive cognitive mood repair response sets each predicted depression outcomes.
Individuals with past and present episodes of depressive disorder report an array of cognitive and non-cognitive responses to their own sadness that are likely to exacerbate that affect, and this pattern predicts a worse course of the disorder.
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